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estradiol 17 beta/brustkrebs

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Enzymatic regulation of estradiol-17 beta concentrations in human breast cancer cells.

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Estradiol-17 beta is known to be involved in both the etiology and maintenance of growth of breast cancer. However, blood levels of the hormone do not reflect those found within the cells due to a number of transformations catalysed by enzymes which may be under metabolite and/or hormonal
Estradiol 17 beta-hydroxysteroid dehydrogenase (E2DH) is the enzyme responsible for the interconversion of estrone (E1), and the more biologically potent steroid, estradiol (E2), and has a crucial role in regulating breast tissue concentrations of E2. It has previously been shown that breast tumor
Estradiol 17 beta-hydroxysteroid dehydrogenase (17 beta HSD) mediates the interconversion of estrone and estradiol in endocrine-responsive tissues such as the breast. The control of 17 beta HSD expression by all-trans-retinoic acid (RA) in T47D breast cancer cells was examined using a specific 17

Selenium, estradiol 17 beta, nitrites, and human breast cancer.

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Breast cancer is the most common cancer in women in the United States. Although there is a large body of studies dealing with selenium, estrogens and nitrites in relation to cancer, most of them are correlated singly and the dynamics of carcinogenesis are overly simplified. The epidemiologic and

Modulation of the estradiol-17 beta mitogenic effect on human breast cancer MCF-7 cells by serum albumin in defined medium.

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The influence of bovine serum albumin on estradiol-17 beta growth and responsiveness of human mammary cancer MCF-7 cells was studied and compared to that of dextran-coated charcoal-treated fetal calf serum and other bovine serum proteins. To reveal the protein factor role, a culture defined medium

Estradiol 17 beta-hydroxysteroid dehydrogenase, a marker of breast cancer hormone dependency.

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Intratumoral activity of the progesterone-dependent enzyme 17 beta-hydroxysteroid dehydrogenase (E2DH) was measured in 114 patients with breast cancer (33 pre- and 81 postmenopausal) before and/or after 8 days of a progestin treatment (lynestrenol, 10 mg/day). In 12 postmenopausal patients, the
We have previously reported that the proliferation of cloned MCF-7 and T47D human mammary tumor cells can be inhibited by increasing concentrations of charcoal-dextran stripped female human serum (CDFHS). The maximal proliferation rate was restored by the addition of 3 X 10(-11) M estradiol-17 beta

A possible discriminant test for hormone-responsive breast cancers. Estradiol--17 beta sensitive dehydrogenase activity.

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The metabolism of 3-H-estradiol-17 beta in human breast cancer in organ culture.

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Sex steroids induced up-regulation of 1,25-(OH)2 vitamin D3 receptors in T 47D breast cancer cells.

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There is evidence indicating that 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] through binding to its specific receptor (VDR) exerts an antiproliferative effect on breast cancer cells. Considering the importance of receptor regulation in modulating the target cell responsiveness to hormones, the effect of
Blood serum levels of sex steroid-binding globulin (SSBG), free and SSBG- and albumin-binding fractions of estradiol-17 beta as well as some indexes of cellular and humoral immunity were compared in 25 young female patients with stage 1-3 breast cancer and controls. No significant difference in SSBG

Comparative histochemical and biochemical assays of estrogen receptors in breast cancer patients.

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Estrogen receptors (ER) in breast cancer tissue were determined in 51 patients by a histochemical method with estradiol-17 beta-bovine serum albumin-fluorescein isothiocyanate conjugate and were compared with those in the adjacent tissue determined by biochemical method, i.e., the sucrose density

Binding of 2-hydroxyestradiol and 4-hydroxyestradiol to estrogen receptors from human breast cancers.

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The binding of catechol estrogens, epoxyenones and methoxyestrogens was evaluated using estrogen receptors in cytosol prepared from human breast cancers. The relative affinity of 2-hydroxyestradiol, a metabolite formed in vitro from estradiol-17 beta by breast cancer cells, was indistinguishable

Effect of adjuvant tamoxifen and CMF on endocrine function of patients with operable breast cancer.

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The effect of adjuvant CMF (cyclophosphamide, methotrexate and 5-fluorouracil) and tamoxifen (TM) on endocrine function was studied in 120 women with stage I-II operable breast cancer. Sixty patients were premenopausal, of whom 25 were treated with CMF for 9 months, 25 received CMF for 9 months + TM
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